Protection of T cells from activation-induced cell death by Fas+ B cells

Eur J Immunol. 2000 Mar;30(3):931-7. doi: 10.1002/1521-4141(200003)30:3<931::AID-IMMU931>3.0.CO;2-H.


Naive CD4+ T cells proliferate strongly in response to stimulation by superantigens such as staphylococcal enterotoxin B (SEB). However, when these same cells revert to a resting phenotype and are subjected to restimulation with either SEB or anti-CD3, the majority of these SEB-responsive cells undergo Fas ligand (FasL)-mediated activation-induced cell death (AICD). We investigated the impact of Fas expression on T cell AICD by utilizing B cell stimulators that lacked functional FasL and either expressed or did not express the Fas receptor. Our results indicate that B cells play an important role in modulating the level of T cell AICD via the Fas/FasL pathway. Activated B cells expressing high levels of Fas receptor can redirect the FasL expressed by T cells primed to undergo AICD away from the T cells and prevent the induction of AICD in these cells. Furthermore, B cells stimulated through both the CD40 receptor and membrane IgM appear to mediate a stronger protective effect on T cells by virtue of their resistance to FasL-mediated cytolysis. These observations suggest a mechanism by which normal B cell and T cell responses to foreign antigen are maintained, while responses to self antigen are not.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigen-Presenting Cells / immunology
  • Apoptosis / immunology*
  • B-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / immunology
  • Enterotoxins / immunology
  • Fas Ligand Protein
  • Lymphocyte Activation*
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred MRL lpr
  • Models, Biological
  • Rats
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology*
  • fas Receptor / metabolism*


  • Enterotoxins
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Faslg protein, rat
  • Membrane Glycoproteins
  • fas Receptor
  • enterotoxin B, staphylococcal